BACKGROUND: For endovascular treatment of vasospasm after aneurysmal subarachnoid hemorrhage (aSAH), an intraarterial treatment course with the calcium channel antagonist nimodipine infused for 30 min is proposed. As some patients still show ongoing vasospasm thereafter, we report on our experience with an extended time period of selective intraarterial nimodipine administration. METHODS: In nine patients with aSAH and refractory cerebral vasospasm, we left the catheter in place within the internal carotid artery after angiography. On the neurosurgical ICU, a continuous infusion of intraarterial nimodipine was commenced, combined with intraarterial heparin anticoagulation. Therapy was controlled with extended neuromonitoring techniques. RESULTS: Three patients died from refractory vasospasm and a fourth suffered lethal sepsis. Three patients survived in a good clinical condition, two of them without apparent neurologic deficit. The efficacy of intraarterial nimodipine was best verified with regional CBF monitoring. TCD failed to detect vasospasm in two patients and missed improvement in four. Brain tissue oxygenation increased in all patients, but was not indicative of vasospasm in one. CT perfusion reflected the treatment course adequately in the qualitative scans. CONCLUSION: Selective continuous intraarterial nimodipine treatment for refractory cerebral vasospasm after aSAH seems feasible and may add to the endovascular therapeutic options. Appropriate monitoring technology is essential for further investigation of this novel technique.
BACKGROUND: For endovascular treatment of vasospasm after aneurysmal subarachnoid hemorrhage (aSAH), an intraarterial treatment course with the calcium channel antagonist nimodipine infused for 30 min is proposed. As some patients still show ongoing vasospasm thereafter, we report on our experience with an extended time period of selective intraarterial nimodipine administration. METHODS: In nine patients with aSAH and refractory cerebral vasospasm, we left the catheter in place within the internal carotid artery after angiography. On the neurosurgical ICU, a continuous infusion of intraarterial nimodipine was commenced, combined with intraarterial heparin anticoagulation. Therapy was controlled with extended neuromonitoring techniques. RESULTS: Three patients died from refractory vasospasm and a fourth suffered lethal sepsis. Three patients survived in a good clinical condition, two of them without apparent neurologic deficit. The efficacy of intraarterial nimodipine was best verified with regional CBF monitoring. TCD failed to detect vasospasm in two patients and missed improvement in four. Brain tissue oxygenation increased in all patients, but was not indicative of vasospasm in one. CT perfusion reflected the treatment course adequately in the qualitative scans. CONCLUSION: Selective continuous intraarterial nimodipine treatment for refractory cerebral vasospasm after aSAH seems feasible and may add to the endovascular therapeutic options. Appropriate monitoring technology is essential for further investigation of this novel technique.
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